Berger R D, Wolff M R, Anderson J H, Kass D A
Department of Internal Medicine, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Circ Res. 1995 Jul;77(1):163-73. doi: 10.1161/01.res.77.1.163.
The mechanism of diastolic pressure elevation induced by acute rapid pacing in pressure-load hypertrophied left ventricles (LVs) remains incompletely understood. It has been ascribed to abnormalities of coronary flow, metabolism, and calcium cycling. However, rapid pacing also alters the timing of atrial and ventricular stimulation relative to the diastolic filling period, and this could also influence diastolic pressures. To test the role of such mechanical factors, LV pressure-volume hemodynamics were measured in closed-chested anesthetized dogs during and after abrupt cessation of rapid atrial pacing. Twenty-one dogs were studied: 6 dogs with LV hypertrophy (LVH) induced by perinephritic hypertension, 5 sham-operated normotensive dogs, and 10 acute normotensive control dogs. In LVH dogs, but not in sham-operated or control dogs, end-diastolic pressure rose progressively with increasing heart rate from 5.6 +/- 3.1 mm Hg at baseline to 22.6 +/- 8.1 mm Hg at 220 beats per minute. In all hearts, rapid pacing shifted the timing of left atrial contraction so that it occurred near the onset of LV filling rather than at end diastole. However, in LVH hearts, early LV diastolic pressure and peak atrial pressure were also markedly elevated. Most striking, immediately after terminating the pacing, diastolic pressure declined to near baseline. This rapid pressure decline occurred just when atrial systole would have ensued and before ventricular activation would have followed had pacing continued. Thus, diastolic pressure elevation resolved before a change in ventricular pacing rate. The role of atrial contraction was further explored by simultaneous atrioventricular pacing. This shifted the time of atrial systole so that it occurred during LV isovolumic contraction, while maintaining the identical LV pacing rate. This change eliminated the diastolic pressure elevation found previously. Further analysis revealed that the pressure increase during rapid pacing was not due simply to partial LV filling imposed on a relaxing ventricle or to hypertension or an intact pericardium. These data indicate that mechanical effects of atrioventricular interaction play an important role in tachycardia-induced diastolic dysfunction in this model of LVH and can be more causative than ischemia or metabolic factors in this setting.
压力负荷性肥厚左心室（LV）急性快速起搏诱发舒张压升高的机制仍未完全明确。其原因一直被归结为冠状动脉血流、代谢及钙循环异常。然而，快速起搏还会改变心房和心室刺激相对于舒张期充盈期的时间，这也可能影响舒张压。为了验证此类机械因素的作用，在开胸麻醉犬快速心房起搏突然停止期间及之后，测量了左心室压力-容积血流动力学。共研究了21只犬：6只由肾周性高血压诱发左心室肥厚（LVH）的犬、5只假手术的正常血压犬以及10只急性正常血压对照犬。在LVH犬中，而非假手术犬或对照犬中，舒张末期压力随心率增加而逐渐升高，从基线时的5.6±3.1 mmHg升至每分钟220次搏动时的22.6±8.1 mmHg。在所有心脏中，快速起搏改变了左心房收缩的时间，使其在左心室充盈开始时而非舒张末期发生。然而，在LVH心脏中，左心室早期舒张压和心房压力峰值也显著升高。最显著的是，起搏终止后，舒张压立即降至接近基线水平。这种快速的压力下降恰好发生在心房收缩本应随之出现之时，且在起搏继续时心室激动本应随后发生之前。因此，舒张压升高在心室起搏频率改变之前就已消退。通过房室同步起搏进一步探究了心房收缩的作用。这改变了心房收缩时间，使其在左心室等容收缩期间发生，同时保持相同的左心室起搏频率。这种改变消除了先前发现的舒张压升高。进一步分析表明，快速起搏期间的压力升高并非仅仅由于在舒张期心室上施加的部分左心室充盈，也不是由于高血压或完整的心包。这些数据表明，房室相互作用的机械效应在该LVH模型的心动过速诱发舒张功能障碍中起重要作用，在此情况下可能比缺血或代谢因素更具因果关系。
